Interpret these echocardiogram findings: normal left ventricular systolic function with ejection fraction 71%, mildly increased left ventricular wall thickness, normal segmental wall motion, normal global longitudinal strain -25.7%, normal right ventricular systolic function (S' 14.4 cm/s, TAPSE 2.9 cm), septal flattening in mid to late diastole consistent with right ventricular volume overload, mildly enlarged right atrium, mild aortic regurgitation (pressure halftime 736 ms), moderate tricuspid regurgitation, severe pulmonary hypertension with estimated pulmonary arterial systolic pressure 62 mmHg, moderate pulmonic regurgitation, enlarged right ventricular outflow tract, dilated inferior vena cava with >50% collapse and elevated right atrial pressure 8 mmHg, and no pericardial effusion.

Echocardiogram Interpretation: Severe Pulmonary Hypertension with Right Ventricular Volume Overload

This echocardiogram demonstrates severe pulmonary hypertension (PASP 62 mmHg) with right ventricular volume overload, moderate tricuspid regurgitation, and compensated right ventricular function; right-heart catheterization is mandatory to differentiate pre-capillary from post-capillary pulmonary hypertension before initiating any therapy. 1

Critical Hemodynamic Findings

Severe Pulmonary Hypertension

• PASP 62 mmHg defines severe pulmonary hypertension (normal <35 mmHg; mild 36-45 mmHg; moderate 46-60 mmHg; severe >60 mmHg). 1
• The dilated inferior vena cava with >50% collapse indicates elevated right atrial pressure of 8 mmHg, confirming hemodynamic significance. 1
• Septal flattening in mid-to-late diastole is pathognomonic for right ventricular volume overload and distinguishes this from pure pressure overload, which causes end-systolic and early diastolic flattening. 2

Right Ventricular Assessment

• TAPSE 2.9 cm and S' 14.4 cm/s meet normal thresholds (TAPSE ≥1.7 cm; S' ≥9.5 cm/s), suggesting preserved RV systolic function. 1
• However, in the presence of moderate tricuspid regurgitation, TAPSE and S' are load-dependent and may overestimate true RV contractility, masking early myocardial dysfunction. 3, 1
• The enlarged right ventricular outflow tract and mildly enlarged right atrium corroborate chronic RV volume overload. 1, 4
• RV longitudinal strain by speckle-tracking should be obtained to provide a load-independent assessment of RV function (normal >23%). 3, 1

Right Heart Chamber Enlargement

• Mildly enlarged right atrium reflects chronic elevation of right atrial pressure from the combination of pulmonary hypertension and moderate tricuspid regurgitation. 4
• Functional tricuspid regurgitation accounts for approximately 80% of significant TR and results from RV enlargement with annular dilatation and leaflet tethering. 4
• The pattern of RV volume overload (septal flattening in mid-to-late diastole) combined with moderate TR indicates that volume overload is the dominant mechanism, rather than pure pressure overload. 2

Left Ventricular Findings

Hyperdynamic Function with Mild Wall Thickening

• Ejection fraction 71% is hyperdynamic; together with mildly increased LV wall thickness, this suggests chronic systemic hypertension or a compensatory response to reduced preload from RV dysfunction. 1, 5
• Global longitudinal strain of -25.7% confirms preserved intrinsic LV myocardial function (normal >-18% to -20%). 3, 1
• The combination of hyperdynamic EF with increased wall thickness requires urgent blood pressure measurement; if ≥130/80 mmHg, aggressive control is needed to prevent progression to heart failure with preserved ejection fraction. 5

Diastolic Function Considerations

• Although not fully reported, the presence of mildly increased LV wall thickness mandates complete diastolic function assessment including E/A ratio, septal and lateral E/e', deceleration time, and pulmonary vein flow patterns. 5
• An E/e' ratio ≥13 or ≥14 indicates elevated LV filling pressures and would suggest post-capillary (Group 2) pulmonary hypertension. 3, 1
• If E/e' is borderline (12-15), a fluid challenge (500 mL saline over 10 minutes) during right-heart catheterization can unmask occult left-heart diastolic dysfunction. 1

Valvular Assessment

Tricuspid Regurgitation

• Moderate TR in severe PH is functional (secondary) and results from annular dilation and leaflet tethering due to RV enlargement. 1, 4
• Semi-quantitative grading requires measurement of vena contracta width and PISA radius; vena contracta ≥7 mm or PISA radius ≥9 mm (Nyquist 28 cm/s) defines severe TR. 3, 1
• Serial echocardiography every 6 months is needed to monitor TR severity, RV dimensions, and PASP. 1

Pulmonic Regurgitation

• Moderate pulmonic regurgitation is a consequence of pulmonary artery dilation from chronic pulmonary hypertension and contributes to RV volume overload. 3

Aortic Regurgitation

• Mild aortic regurgitation with pressure half-time 736 ms is hemodynamically insignificant (severe AR has PHT <200 ms). 3, 1

Mandatory Diagnostic Algorithm

Step 1: Right-Heart Catheterization (Class I Indication)

• Perform RHC immediately to measure mean PAP, pulmonary capillary wedge pressure (PCWP), and calculate pulmonary vascular resistance. 1
• PCWP ≤15 mmHg indicates pre-capillary PH (Group 1); PCWP >15 mmHg indicates post-capillary PH (Group 2). 1
• If PCWP is borderline (12-15 mmHg), perform a fluid challenge during catheterization to unmask occult left-heart diastolic dysfunction. 1
• Non-invasive estimates cannot reliably differentiate pre- from post-capillary PH, a distinction essential for appropriate therapy. 1

Step 2: Complete Echocardiographic Diastolic Assessment

• Measure E/A ratio, septal and lateral E/e', deceleration time, and pulmonary vein flow patterns. 1, 5
• Calculate left atrial volume index; values ≥34 mL/m² confirm chronic diastolic dysfunction and suggest Group 2 PH. 3, 5
• Quantify TR severity with vena contracta and PISA measurements to document baseline for longitudinal monitoring. 3, 1

Step 3: Etiologic Work-Up Based on RHC Results

If Pre-Capillary PH (Group 1) Confirmed:

• Screen for connective tissue disease (ANA, anti-Scl-70, anti-centromere), HIV, liver function tests, and ventilation-perfusion scan to exclude chronic thromboembolic PH. 1
• Consider pulmonary function tests, high-resolution CT, and arterial blood gases to evaluate for Group 3 lung disease. 1

If Post-Capillary PH (Group 2) Confirmed:

• Measure blood pressure urgently and optimize control. 1, 5
• Complete diastolic function assessment as above. 1
• Consider cardiac MRI if infiltrative cardiomyopathy is suspected (wall thickness disproportionate to hypertension, unexplained LV stiffness). 5

Management Strategy

Pulmonary Hypertension-Specific Therapy

• Do NOT start endothelin-receptor antagonists, phosphodiesterase-5 inhibitors, or prostacyclins until RHC confirms pre-capillary PH (Group 1). 1
• PAH-specific drugs are contraindicated (Class III) in Group 2 PH and may precipitate pulmonary edema. 1
• If post-capillary PH is diagnosed, optimize treatment of underlying left-heart disease with blood pressure control and diuretics as needed. 1

Right Ventricular Support

• Avoid excessive diuresis that could reduce RV preload and trigger hemodynamic collapse. 1
• Maintain adequate systemic arterial pressure to preserve RV coronary perfusion; systemic vasodilators should be avoided. 1
• Monitor volume status carefully; the dilated IVC with >50% collapse indicates adequate preload, but this can change rapidly. 1

Tricuspid Valve Intervention

• Surgical or transcatheter tricuspid valve repair/replacement is NOT indicated for functional TR unless it is severe (vena contracta ≥7 mm, EROA ≥40 mm²) and the patient remains symptomatic despite optimal medical therapy. 1
• Current moderate TR should be monitored with serial echocardiography every 6 months. 1

Critical Pitfalls to Avoid

• Do not rely solely on TAPSE 2.9 cm and S' 14.4 cm/s to declare normal RV function in the presence of moderate TR; these parameters are load-dependent and may be falsely reassuring. 3, 1
• Do not initiate PAH-specific vasodilator therapy without confirming pre-capillary PH by RHC; doing so in Group 2 PH can be harmful. 1
• Do not overlook the discordance between severe PH (PASP 62 mmHg) and apparently normal RV systolic function; this pattern indicates early compensated disease that may deteriorate without timely treatment. 1
• Do not dismiss hyperdynamic EF (71%) with mild LV wall thickening as benign; it may reflect uncontrolled systemic hypertension driving diastolic dysfunction and post-capillary PH. 1, 5
• Do not delay right-heart catheterization; the distinction between pre- and post-capillary PH is essential and cannot be made reliably by echocardiography alone. 1
• Do not assume the septal flattening pattern alone determines the etiology; mid-to-late diastolic flattening indicates volume overload, but the underlying cause of PH still requires invasive confirmation. 2

{"question": "Interpret these echocardiogram findings: normal left ventricular systolic function with ejection fraction 71%, mildly increased left ventricular wall thickness, normal segmental wall motion, normal global longitudinal strain -25.7%, normal right ventricular systolic function (S' 14.4 cm/s, TAPSE 2.9 cm), septal flattening in mid to late diastole consistent with right ventricular volume overload, mildly enlarged right atrium, mild aortic regurgitation (pressure halftime 736 ms), moderate tricuspid regurgitation, severe pulmonary hypertension with estimated pulmonary arterial systolic pressure 62 mmHg, moderate pulmonic regurgitation, enlarged right ventricular outflow tract, dilated inferior vena cava with >50% collapse and elevated right atrial pressure 8 mmHg, and no pericardial effusion."}